DESCRIPTION Studies indicate that environmental tobacco smoke (ETS) may be a significant risk factor for coronary atherosclerotic heart disease (CAD). In addition, several studies showed the association between ETS and increase in ROS production although the precise mechanism has not been determined. Importantly, the possible role of ROS in atherogenesis has been demonstrated in many studies. Since mitochondria is the major source of ROS production, the proposed study hypothesized that ETS may induce an increase in ROS production that may further induce lipid peroxidation and mitochondrial DNA (mt DNA) damage resulting in oxidative phosphorylation (OXPHOS) inhibition. To test this hypothesis, it is proposed to demonstrate that ETS induces genetic damage, somatic mutation, and lipid peroxidation in cardiovascular tissue from apoE(-/-) transgenic and control apoE(+/+) mice. They further proposed to determine whether ETS mediated atherogenesis in the apoE(-/-) is associated with increased ROS production, mit DNA damage and lipid peroxidation.